Surgical infections

Dr. AHMED M. 1
Outlines
• Introduction
• Classification of surgical wounds
• Causes and risk factors
• Preventions
• Prophylactic antibiotics
• Treatment

2
Introduction
• Definitions:
• I. Surgical infections are those that occur as a result of a surgical
procedure or those that require surgical intervention.
• They are characterized by a breach of mechanical/anatomic
defense mechanisms (barriers)

• II. Surgical Site Infections(SSI)

• SSIs are infections present in any location along the surgical tract
after a surgical procedure
• Occurs within 30 days after surgery or within 1 year if a prosthetic
implant is in place.
3
Cont…
• Infection is characterized by cardinal signs of inflammation or
dehiscence and by purulent drainage.
• Other indicators of infection include fever, deliberate opening
of the wound, culture-positive drainage, and a physician's
diagnosis of infection with prescription of antibiotics
• III. Contamination is the presence of bacteria without
multiplication.
• IV. Colonization is multiplication without host response.
• V. Infection is the presence of host response in reaction to
deposition and multiplication of bacteria.

4
Localized surgical infection
Cellulitis, erysipelas and skin abscess
• Cellulitis (which includes erysipelas) manifests as an area of
skin erythema, edema, and warmth; it develops as a result of
bacterial entry via breaches in the skin barrier
• A skin abscess is a collection of pus within the dermis or
subcutaneous space.
• Cellulitis is observed most frequently among middle-aged
individuals and older adults
• Erysipelas occurs in young children and older adults
• Skin abscess may occur in healthy individuals with no
predisposing conditions.
5
• Predisposing factors for development of cellulitis and/or skin abscess
include
 Skin barrier disruption due to trauma (such as abrasion, penetrating
wound, pressure ulcer, venous leg ulcer, insect bite, injection drug use)
 Skin inflammation (such as eczema, radiation therapy)
 Edema due to impaired lymphatic drainage
 Edema due to venous insufficiency

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 Obesity
 Immunosuppression (such as diabetes or HIV infection)

Abdominal trauma
 Breaks in the skin between the toes ("toe web intertrigo"); these may be
clinically inapparent
 Preexisting skin infection (such as tinea pedis, impetigo, varicella)
• Cellulitis and erysipelas — The most common cause of cellulitis is
 beta-hemolytic streptococci (groups A, B, C, G, and F), most commonly group A
Streptococcus or Streptococcus pyogenes;
 S. aureus (including methicillin-resistant strains) is a notable but less common
cause
 Gram-negative aerobic bacilli are identified in a minority of cases. 6
• Skin abscess — The most common cause of skin abscess is S. aureus
(either methicillin-susceptible or methicillin-resistant S. aureus), which
CLINICAL MANIFESTATIONS
• Cellulitis and erysipelas manifest as areas of skin erythema, edema,
and warmth; they develop as a result of bacterial entry via breaches
in the skin barrier
• Cellulitis and erysipelas are nearly always unilateral, and the lower

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extremities are the most common site of involvement
Cellulitis Erysipelas

 involves the deeper dermis and
subcutaneous fat
 may present with or without
purulence
 tend to have a more indolent
course with development of
localized symptoms over a few
days.
Abdominal trauma
 involves the upper dermis and
superficial lymphatics
 is nonpurulent
 tend to have acute onset of
symptoms with systemic
manifestations including fever
and chills
 lesions are raised above the
level of surrounding skin with 7
clear demarcation between
involved and uninvolved tissue
8

Abdominal trauma 04/03/2024

• Skin abscess
• A skin abscess is a collection of pus within the dermis or

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subcutaneous space
• manifests as a painful, fluctuant, erythematous nodule, with or
without surrounding cellulitis

Abdominal trauma
• Spontaneous drainage of purulent material may occur.
• Regional adenopathy may be observed
• A skin abscess may develop via deep infection of a hair follicle
(known as a furuncle or boil), which reflects extension of purulent
material through the dermis into the subcutaneous tissue.
• Multiple furuncles can coalesce to form carbuncles ,which may be
associated with systemic symptoms. 9
• Common areas of involvement include the back of the neck, face,
axillae, and buttocks
• Complications — Complications of cellulitis and abscess include
 bacteremia,

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 endocarditis,
 osteomyelitis,
 metastatic infection,

Abdominal trauma
 sepsis, and
 toxic shock syndrome
• DIAGNOSIS — The diagnosis of cellulitis, erysipelas, and skin abscess is
usually based upon clinical manifestations.
 Cellulitis and erysipelas manifest as areas of skin erythema, edema, and
warmth
 Erysipelas lesions are raised above the level of surrounding skin with clear
demarcation between involved and uninvolved tissue
 A skin abscess manifests as a painful, fluctuant, erythematous nodule, with or 10
without surrounding cellulitis
• Laboratory testing is not required for patients with uncomplicated
• Blood cultures are warranted for patients in the following
circumstances and should be obtained prior to the initiation of
antibiotic therapy
Systemic toxicity
Extensive skin or soft tissue involvement

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Underlying comorbidities (lymphedema, malignancy, neutropenia,
immunodeficiency, splenectomy, diabetes)
Special exposures (animal bite, water-associated injury)

Abdominal trauma
Persistent cellulitis
• Radiographic evaluation may be warranted in patients with underlying
conditions such as
diabetes,
venous insufficiency, or lymphedema and
in patients with persistent systemic symptoms.
• Radiographic examination can be useful to determine whether a skin 11
abscess is present (via ultrasonography) and for distinguishing cellulitis
from osteomyelitis (via magnetic resonance imaging)
Treatment
Elevation if extremity is involved
Patients with nonpurulent infection (ie, cellulitis or erysipelas in the
absence of abscess or purulent drainage) should be managed with
empiric antibiotic therapy

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Patients with drainable abscess should undergo incision and drainage; .
In addition, antibiotic therapy is warranted if clinical criteria are met,
Patients with purulent cellulitis (ie, cellulitis associated with purulent

Abdominal trauma
drainage in the absence of drainable abscess) should be managed with
antibiotic therapy
 Oral versus parenteral therapy — Patients with mild infection may be
treated with oral antibiotics. Treatment with parenteral antibiotics is
warranted in the following circumstances:
 Systemic signs of toxicity (eg, fever >100.5°F/38°C, hypotension, or sustained
tachycardia)
 Rapid progression of erythema
 Progression of clinical findings after 48 hours of oral antibiotic therapy 12
 Inability to tolerate oral therapy
 Proximity of the lesion to an indwelling medical device (eg, prosthetic joint or
vascular graft)
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 Pyomyositis
• Pyomyositis is a purulent infection of skeletal muscle that arises from
hematogenous spread, usually with abscess formation

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• Pyomyositis is classically an infection of the tropics, although it has
been recognized in temperate climates with increasing frequency
• Tropical pyomyositis primarily occurs in two age groups: children
(ages 2 to 5) and adults (ages 20 to 45), while the majority of
temperate pyomyositis cases occurs in adults
• Males appear to be more commonly affected than females
• Most patients with tropical pyomyositis are otherwise healthy
without underlying comorbidities, while most patients in temperate
regions are immunocompromised or have other serious underlying
conditions. 18
 Predisposing factors
• Immunodeficiency (HIV infection, diabetes mellitus, malignancy,
cirrhosis, renal insufficiency, organ transplantation, and

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administration of immunosuppressive agents)
• Trauma
• Injection drug use

Abdominal trauma
• Concurrent infection ( Toxocariasis:because of predisposing muscle
damage and impaired local immunity )
• malnutrition

19
MICROBIOLOGY
• Staphylococcus aureus is the most common cause of
pyomyositis; it causes up to 90 percent of tropical cases and

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up to 75 percent of temperate cases
• Methicillin-resistant S. aureus (MRSA), including community-
acquired strains, is also an increasingly important pathogen

Abdominal trauma
• Group A streptococci is the second most common pathogen.
• Less common causes include non-group A streptococci,
pneumococci, and gram-negative enteric bacilli
• Pyomyositis can also be polymicrobial, particularly in diabetic
patients
• Escherichia coli pyomyositis is an emerging infection among
patients with hematologic malignancy 20
CLINICAL MANIFESTATIONS
• Pyomyositis presents with fever and pain with cramping
localized to a single muscle group.

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• The disease occurs most often in the lower extremity (sites
include the thigh, calf, and gluteal muscles) but any muscle
group can be involved, including the iliopsoas, pelvic, trunk,

Abdominal trauma
paraspinal, and upper extremity muscles
• Mortality due to pyomyositis was reported to be as high as 10
percen
• Pyomyositis can be divided into three clinical stages

21
• Stage 1
 characterized by crampy local muscle pain, swelling, and low-grade fever.
 Mild leukocytosis and induration of the affected muscle may be present
 A deep abscess may not be discretely palpable, but the muscle may have a
"woody" texture on palpation
 Fluctuation is not present, and aspiration of the muscle will not yield purulent
material.

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• Stage 2
 occurs 10 to 21 days after the initial onset of symptoms

Abdominal trauma
 characterized by fever, exquisite muscle tenderness, and edema
 A frank abscess may be clinically apparent, and aspiration of the affected
muscle typically yields pus
 Marked leukocytosis is usually present.
 More than 90 percent of the patients present at this suppurative stage.
• Stage 3
 characterized by systemic toxicity
 The affected muscle is fluctuant
 Complications of S. aureus bacteremia such as septic shock, endocarditis, 22
septic emboli, pneumonia, pericarditis, septic arthritis, brain abscess, and
acute renal failure can occur
DIAGNOSIS
• Tools for diagnosis of pyomyositis include radiography, cultures, and
laboratory data.
• Radiography :imaging is the most useful tool for diagnosing
pyomyositis, defining the site(s) of infection, and for ruling out other

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entities
 If available, magnetic resonance imaging (MRI) is the optimal imaging
technique

Abdominal trauma
 It is highly sensitive for muscle inflammation, even prior to the formation
of a frank abscess,
 and can demonstrate the extent of involvement in the tissues.
 If MRI is not available, computed tomography (CT) is helpful for detecting
muscle swelling and well-delineated areas of fluid attenuation that display
rim enhancement with contrast, as well as for radiographic-guided
drainage of purulent material
 Ultrasonography is also a potentially useful diagnostic and therapeutic tool,
particularly during the purulent stage of infection when it may reveal 23
diffuse muscle hyperechogenicity with or without localized hypoechogenicity
and diffuse hyperemia
• Cultures:
 Bacteriologic diagnosis can be made by cultures of drainage

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specimens.
 Diagnostic drainage prior to antibiotic therapy is helpful for obtaining
optimal microbiologic data and susceptibility testing to direct specific

Abdominal trauma
therapy.
 Blood cultures are positive in up to 10 percent of tropical cases and
35 percent of temperate cases
• Laboratory data:
 Nonspecific laboratory findings include leukocytosis with left shift
 and elevated inflammatory markers (erythrocyte sedimentation rate
and C-reactive protein).
 Eosinophilia should raise suspicion for a concomitant parasitic
infection 24
 Counterintuitively, creatine kinase levels are often normal
TREATMENT
• although stage 1 pyomyositis can be treated with antibiotics alone,
most patients present with stage 2 or 3 disease and therefore require
both antibiotics and drainage for definitive management

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• Drainage :
• Image-guided percutaneous drainage is an option for many
patient(can be useful both to secure a microbiologic diagnosis early

Abdominal trauma
in patient evaluation and as a therapeutic measure when combined
with antimicrobial therapy)
• Percutaneous drainage is often computed tomography (CT) guided,
but, in selected patients, an ultrasound (US)-guided procedure is an
option
• surgical intervention may be required In the setting of deep infection
or extensive muscle involvement with significant necrosis
25
• Regardless of the type of drainage procedure done, antimicrobial
therapy should be initiated without delay in patients who present
with systemic toxicity
Antibiotics
• for immunocompetent individuals, initial empiric parenteral
antibiotic therapy should be directed against staphylococci, including
methicillin-resistant S. aureus (MRSA) and streptococci

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Abdominal trauma
26
• For immunocompromised individuals, broad antibiotic coverage for
gram-positive, gram-negative, and anaerobic organisms should be
administered. In such circumstances, vancomycin may be combined
with a broad-spectrum regimen that has activity against gram
negatives and anaerobes

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Abdominal trauma
27
 Clindamycin is sometimes included in the antibiotic regimen for severe
infections due to S. aureus or beta-hemolytic streptococci because it has
several unique characteristics
 suppresses synthesis of bacterial toxins and penicillin-binding proteins,
which are involved in cell wall synthesis and degradation

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 has a longer post-antibiotic effect compared with beta-lactams,
 is not affected by bacterial inoculum size or stage of growth

Abdominal trauma
 do not routinely use it for this purpose in the absence of necrotizing
infection or concern for toxic shock syndrome
 the duration of antimicrobial therapy should be tailored to clinical and
radiographic improvement.
 Three to four weeks of parenteral therapy is usually sufficient
 patients with extensive, multifocal, or poorly drained infection may warrant
longer courses of therapy
 The course of therapy for patients with other sequelae of bacteremia (such
as endocarditis or osteomyelitis) should be adjusted based on the nature of 28
infection at these other sites
 In rare cases of infections caused by mycobacteria, the nature and duration
 Clostridial myonecrosis(gas
gangrene)
• is a life-threatening muscle infection that develops either contiguously
from an area of trauma or hematogenously from the gastrointestinal

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tract with muscle seeding
• There are two major presentations of clostridial gas gangrene:
traumatic and spontaneous.

Abdominal trauma
• Traumatic gas gangrene is most commonly caused by Clostridium
perfringens; spontaneous gangrene is most commonly caused by
Clostridium septicum.
• Clostridium species are widespread in nature due to their ability to
form endospore
• they are commonly found in soil and marine sediments as well as
human and animal intestinal tracts. 29
• Categories of clostridial soft tissue infections include wound
contamination, anaerobic cellulitis, myonecrosis (gas gangrene), and
• Wound contamination with soil containing clostridial spores or
vegetative organisms may occur(30 to 80 percent of open traumatic
wounds were contaminated with clostridial species)

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 although contamination with clostridial species in the absence of devitalized
tissue does not necessarily lead to infection.
• Anaerobic cellulitis occurs in the setting of modest quantities of

Abdominal trauma
devitalized tissue that support the growth of C. perfringens or other
clostridial strains
 Gas is produced locally and extends along fascial planes
 bacteremia and invasion of healthy tissue (including muscle) does not occur.
 Mortality is low in the setting of appropriate management, including prompt
removal of the devitalized tissue
• Myonecrosis (clostridial gas gangrene) may be distinguished from
the above infections by the progressive invasion and destruction of
30
healthy muscle tissue
 There are two major presentations of clostridial gas gangrene: traumatic and
spontaneous
Traumatic gas gangrene
• Traumatic wounds with vascular compromise (particularly deep
penetrating injuries such as knife wounds, gunshot wounds, and
crush injuries) create an anaerobic environment that is ideal for
proliferation of clostridia.

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• Traumatic injury accounts for about 70 percent of gas gangrene
cases, and about 80 percent of these are caused by C. perfringens

Abdominal trauma
• Other pathogens include C. septicum, C. novyi, C. histolyticum, C.
bifermentans, C. tertium, and C. fallax.
• Gas gangrene caused by C. perfringens continues to occur among
victims of natural disasters with delayed evacuation and treatment

31
• Conditions associated with traumatic gas gangrene include:
• Bowel and biliary tract surgery
• Gunshot wounds, knife wounds

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• Compound fractures
• Abortion
• Retained placenta

Abdominal trauma
• Prolonged rupture of the membranes
• Intrauterine fetal demise
• Intramuscular injection
• Black tar heroin injection (skin popping)
• Pathogenesis —Trauma introduces organisms (vegetative or spore forms)
directly into deep tissue. If trauma compromises the blood supply, an
anaerobic environment forms with low oxidation-reduction potential and
acidic pH, which is optimal for growth of clostridial organisms .
• Necrosis progresses within 24 to 36 hours of the traumatic injury. 32
• Many extracellular toxins are produced by C. perfringens; of these, alpha
and theta toxins have been implicated in pathogenesis
Clinical manifestations
• Traumatic gas gangrene usually presents with sudden onset of severe
pain at the site of surgery or trauma .
• The mean incubation period is less than 24 hours (range 6 hours to
several days), depending on the size of the bacterial inoculum and the

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extent of vascular compromise.
• Pain is likely related to toxin-mediated ischemia.
• The skin over the infected area initially may appear pale then rapidly

Abdominal trauma
develops a bronze appearance, followed by purple or red
discoloration. The skin becomes tense and exquisitely tender.
Overlying bullae may be clear, red, blue, or purple
• Signs of systemic toxicity develop rapidly including tachycardia and
fever, followed by shock and multiorgan failure
• Bacteremia occurs in about 15 percent of cases and may be
associated with brisk intravascular hemolysis 33
• Additional complications of clostridial myonecrosis include jaundice,
renal failure, hypotension, and liver necrosis
 Diagnosis
• Pain at a site of traumatic injury together with signs of systemic toxicity and
gas in the soft tissue support the diagnosis of gas gangrene.

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• Physical evidence of crepitus in the soft tissue is the most sensitive and
specific finding on clinical examination
• Radiographic imaging

Abdominal trauma
 can be especially useful for identifying gas in deep tissues(Gas within the soft tissue
can be detected by radiography, computerized tomographic (CT) scan, or magnetic
resonance imaging (MRI))
 Early in the course of infection, CT and MRI are useful for determining if the infection
is localized or spreading along fascial planes.
• Culture
 Blood (both aerobic and anaerobic bottles) and tissue cultures should be obtained;
definitive diagnosis of gas gangrene requires demonstration of large gram-variable
rods at the site of injury
 Clostridia can appear both gram positive and gram negative when stained directly 34
from infected tissues but stain as gram-positive rods when obtained from culture
media
 Drainage from surgical procedures is characteristically absent of frank pus, and
Surgical exploration
 in the setting of traumatic gas gangrene typically demonstrates

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muscle that does not bleed or contract when stimulated.
 Muscle tissue is grossly edematous and may have reddish-blue to
black discoloration.

Abdominal trauma
 Microscopic evaluation of biopsy material invariably
demonstrates organisms among degenerating muscle bundles
and a characteristic absence of acute inflammatory cells
 In the presence of muscle necrosis, necrosis of skin, fat,
subcutaneous tissue, and fascia may also be present.

35
Treatment
• Treatment of traumatic gas gangrene consists of
 surgical debridement, antibiotic therapy, andsupportive measures.
 Prompt, aggressive, and thorough surgical inspection and debridement of devitalized tissue are
mandatory to improve survival, preserve limbs, and prevent complications
• Pending definitive etiologic diagnosis, broad-spectrum empiric antibiotic treatment
is warranted to cover

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 group A Streptococcus, Clostridium species, and mixed aerobes and anaerobes.
• Options include either
 piperacillin-tazobactam or ticarcillin-clavulanate ,
 PLUS clindamycin .

Abdominal trauma
 Carbapenems are an acceptable alternative choice.
• Definitive antibiotic therapy should consist of the combination of
(clindamycin and tetracycline have the ability to inhibit toxin synthesis)
 penicillin
 plus clindamycin or
 tetracycline
• Prognosis — The prognosis for gas gangrene of an extremity is more favorable than
gas gangrene of the trunk or visceral organs, since gangrene of an extremity may be
debrided more readily 36
• Patients with associated bacteremia and intravascular hemolysis have the greatest
likelihood of progressing to shock and death
Spontaneous gas gangrene
• Spontaneous gas gangrene generally occurs via hematogenous seeding of muscle
with bacteria (usually C. septicum) from a gastrointestinal tract portal of entry.
• Pathogenesis : C. septicum can grow in normal tissues; it does not require
anaerobic conditions. The presence of a gastrointestinal lesion facilitates entry of
the organism into the bloodstream and then into other tissues

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• C. septicum produces multiple exotoxins, including [1]:
 Alpha toxin (a lethal, hemolytic, necrotizing toxin)
 Beta toxin (DNase)
 Gamma toxin (hyaluronidase)

Abdominal trauma
 Delta toxin (septicolysin, an oxygen labile hemolysin)
 A protease
 A neuraminidase
• Clinical manifestations :
 Spontaneous gas gangrene usually presents with abrupt onset of severe muscle pain
 Occasionally, heaviness or numbness is reported
 In some patients, the first manifestation may be confusion or malaise
 Infection progresses rapidly with development of edema and bullae filled with clear,
cloudy, hemorrhagic, or purplish fluid.
 The skin around the bullae has a purple hue, perhaps reflecting vascular compromise 37
resulting from bacterial toxins diffusing into surrounding tissues
 Histopathology of muscle and connective tissues demonstrates cell lysis and gas formation;
inflammatory cells are absent
• Predisposing factors include:
 Colonic malignancy

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 Inflammatory bowel disease
 Diverticulitis
 Gastrointestinal surgery

Abdominal trauma
 Leukemia
 Lymphoproliferative disorders
 Chemotherapy
 Neutropenia
 Radiation therapy
 AIDS
 Necrotizing enterocolitis, cecitis, or distal ileitis 38
Diagnosis
• Fever and severe pain in an extremity (in the absence of trauma) should
raise suspicion for spontaneous gas gangrene
• Distinguishing spontaneous gas gangrene due to clostridia from
streptococcal myositis may be difficult

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• The presence of tissue crepitus favors clostridial infection
• Gas within the soft tissue can also be detected by radiography, CT scan,
or MRI.

Abdominal trauma
• Definitive diagnosis of spontaneous gas gangrene requires
demonstration of large gram-variable rods at the site of injury.
• Gram stain of bullous fluid may also be useful.
• Blood cultures should also be obtained since bacteremia in C. septicum
gangrene usually precedes cutaneous manifestations by several hours
• Surgical findings are as described for traumatic gas gangrene
• Treatment — Treatment of spontaneous gas gangrene consists of early
39
surgical debridement and antibiotic therapy. Urgent, thorough surgical
debridement is mandatory to improve survival, preserve limbs, and
prevent complications
Treatment
 Treatment of spontaneous gas gangrene consists of early surgical debridement and
antibiotic therapy.
 Pending definitive etiologic diagnosis, broad-spectrum empiric antibiotic treatment is
warranted to cover
 group A Streptococcus,

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 Clostridium species, and
 mixed aerobes and anaerobes Options include either
 piperacillin-tazobactam or
 ticarcillin-clavulanate , PLUS

Abdominal trauma
 clindamycin
 Antibiotic therapy for treatment of spontaneous gas gangrene due to C. septicum
combination of
 penicillin plus
 clindamycin or
 tetracycline
 C. tertium is resistant to penicillin, cephalosporins, and clindamycin. Appropriate is
 vancomycin or
 metronidazole
 Patients who survive spontaneous gangrene should have colonoscopy to rule out
associated pathology of the gastrointestinal tract. 40
 Prognosis —
 The mortality of spontaneous gangrene ranges from 67 to 100 percent .
 The majority of deaths occur within 24 hours of onset.
Necrotizing soft tissue infections
• Necrotizing soft tissue infections (NSTI) include necrotizing forms of
fasciitis, myositis, and cellulitis ;characterized clinically by
 fulminant tissue destruction,
 systemic signs of toxicity, and
 high mortality

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• organisms that cause NSTI as "flesh-eating bacteria
• Necrotizing infection may be categorized based on microbiology and

Abdominal trauma
presence or absence of gas in the tissues
1. Necrotizing fasciitis
• an infection of the deep soft tissues that results in progressive destruction
of the muscle fascia and overlying subcutaneous fat
• Infection typically spreads along the muscle fascia due to its relatively poor
blood supply; muscle tissue is frequently spared because of its generous
blood supply
• Development of anesthesia may precede the appearance of skin necrosis
41
and provide a clue to the presence of necrotizing fasciitis
• Initially, the overlying tissue can appear unaffected; therefore, necrotizing
fasciitis is difficult to diagnose without direct visualization of the fascia.
• Necrotizing fasciitis may be divided into two microbiologic categories:
I. Polymicrobial (type I) necrotizing infection is caused by aerobic and
anaerobic bacteria
Typically,

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 at least one anaerobic species (most commonly Bacteroides, Clostridium, or
Peptostreptococcus) is isolated combination with
 Enterobacteriaceae (eg, Escherichia coli, Enterobacter, Klebsiella, Proteus)

Abdominal trauma
and
 one or more facultative anaerobic streptococci (other than group A
Streptococcus [GAS])
 Obligate aerobes (such as Pseudomonas aeruginosa) are rarely components
of such mixed infections
• usually occurs in older adults and/or in individuals with underlying
comorbidities
• The most important predisposing factor is diabetes, especially with
associated peripheral vascular disease 42
II. Monomicrobial (type II) necrotizing infection
• is usually caused by GAS or other beta-hemolytic streptococci.
• Infection may also occur as a result of Staphylococcus aureus
• may occur in any age group and in individuals with no underlying
comorbidities
2. Necrotizing myositis
• is an infection of skeletal muscle typically caused by group A

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Streptococcus (and other beta-hemolytic streptococci
• may be preceded by skin abrasions, blunt trauma, or heavy exercise
3. Necrotizing cellulitis

Abdominal trauma
• is typically caused by anaerobic pathogens and may be divided into two
types:
• clostridial (usually caused by Clostridium perfringens; less frequently
Clostridium septicum) and
• nonclostridial (caused by polymicrobial infection).
• In both types, crepitus is observed in the skin, but there is sparing of the
fascia and deep muscles
• Pain, swelling, and systemic toxicity are not prominent features, and the
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relative mildness helps distinguish cellulitis from clostridial myonecrosis (gas
gangrene
RISK FACTORS
• Risk factors for NSTI include
 Major penetrating trauma
 Minor laceration or blunt trauma (muscle strain, sprain, or contusion)
 Skin breach (varicella lesion, insect bite, injection drug use)

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 Recent surgery (including colonic, urologic, and gynecologic procedures as
well as neonatal circumcision)
 Mucosal breach (hemorrhoids, rectal fissures, episiotomy)

Abdominal trauma
 Immunosuppression (diabetes, cirrhosis, neutropenia, HIV infection)
 Malignancy
 Obesity
 Alcoholism
 In women: pregnancy, childbirth, pregnancy loss, gynecologic procedures
• Diabetes is a particularly important risk factor for necrotizing
infection involving the lower extremities, perineum, and head and
neck region
44
CLINICAL MANIFESTATIONS
• Necrotizing infection most commonly involves the extremities (lower
extremity more commonly than upper extremity)
• Necrotizing infection usually presents acutely (over hours); rarely, it

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may present subacutely (over days).
• Rapid progression to extensive destruction can occur, leading to
systemic toxicity, limb loss, and/or death

Abdominal trauma
• Clinical manifestations of necrotizing infection include
 Erythema (without sharp margins)
 Edema that extends beyond the visible erythema
 Severe pain (out of proportion to exam findings in some cases)
 Fever
 Crepitus
 Skin bullae, necrosis, or ecchymosis
 tachycardia, and 45
 systemic toxicity may be observed
 Hypotension
46
• The subcutaneous tissue may be firm and indurated, such that the
underlying muscle groups cannot be palpated distinctly

04/03/2024
• The process progresses rapidly over several days, with changes in
skin color from red-purple to patches of blue-gray. Within three to
five days after onset, skin breakdown with bullae (containing thick

Abdominal trauma
pink or purple fluid) and frank cutaneous gangrene can be seen
• In the setting of surgical wound infection, NSTI is characterized by
copious drainage, dusky and friable subcutaneous tissue, and pale,
devitalized fascia
• diminished sensation to pain develops in the involved area, due to
thrombosis of small blood vessels and destruction of superficial
nerves in the subcutaneous tissue. This may precede the
appearance of skin necrosis and provide a clue to the presence of
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necrotizing fasciitis
• The diagnosis of necrotizing infection is established via surgical
exploration of the soft tissues in the operating room, with

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physical examination of the skin, subcutaneous tissue, fascial
planes, and muscle
• Surgical exploration is required to establish the presence of

Abdominal trauma
necrotizing infection, evaluate the scope of involvement, and to
debride devitalized tissue
• intraoperative specimens should be sent for Gram stain and
culture (in addition to histology)
• Radiographic imaging studies can be useful to help determine
whether necrotizing infection is present but should not delay
surgical intervention
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• Blood cultures (two sets) should be obtained prior to
administration of antimicrobial therapy.
• Clinical factors that may make diagnosis of NSTI difficult include
• Absence of fever
• Absence of cutaneous manifestations
• Attribution of severe pain to alternative cause

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• Nonspecific imaging tests
• Attributing systemic manifestations to other causes
Surgical exploration and debridement — Surgical exploration is the only

Abdominal trauma
way to establish the diagnosis of necrotizing infection. Findings on direct
examination include swollen and dull-gray appearance of the fascia, thin
exudate without clear purulence, and easy separation of tissue planes by
blunt dissection
Early debridement is associated with better outcomes; survival is
significantly increased among patients taken to surgery within 24 hours
after admission
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Characteristic pathologic features of necrotizing fasciitis include extensive
tissue destruction, thrombosis of blood vessels, abundant bacteria
spreading along fascial planes, and infiltration of acute inflammatory cells
• Radiographic imaging
• The best initial radiographic imaging exam is computed tomography
(CT) scan
• The most useful finding is presence of gas in soft tissues,
• this finding is highly specific for necrotizing soft tissue infection and

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should prompt immediate surgical intervention
• Other radiographic findings may include fluid collections, absence or

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heterogeneity of tissue enhancement with intravenous contrast, and
inflammatory changes beneath the fascia.
• Frequently, imaging studies demonstrate soft tissue swelling; this
finding is not specific since it is not possible to distinguish between
swelling caused by infection, trauma, surgery, or inflammation.
Therefore, in such cases, the diagnosis of necrotizing infection can be
established only by surgical exploration.
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TREATMENT
 Treatment of necrotizing infection consists of early and aggressive surgical
exploration and debridement of necrotic tissue, together with broad-
spectrum empiric antibiotic therapy and hemodynamic support.

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 Administration of antibiotic therapy in the absence of debridement is
associated with a mortality rate approaching 100 percent
Surgical debridement :

Abdominal trauma
 Necrotizing soft tissue infection is a surgical emergency.
 Radiographic imaging studies should not delay surgical intervention when
there is crepitus on examination or rapid progression of clinical manifestations
 The goal of operative management is to perform aggressive debridement of
all necrotic tissue until healthy, viable (bleeding) tissue is reached.
 Inspection and debridement in the operating room should be continued every
one to two days until necrotic tissue is no longer present
 For severe necrotizing infection involving the extremities, amputation may be
needed to control the infection 51
• Antibiotic therapy
 empiric treatment of necrotizing infection should consist of broad-spectrum
antimicrobial therapy, including activity against gram-positive, gram-negative, and
anaerobic organisms
 Antibiotic therapy should be initiated promptly after obtaining blood cultures
• Acceptable empiric antibiotic regimens include
 A carbapenem or beta-lactam-beta-lactamase inhibitor plus
 An agent with activity against methicillin-resistant S. aureus (MRSA; such as vancomycin

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or linezolid)
 Clindamycin, for its antitoxin effects against toxin-elaborating strains of streptococci and
staphylococci
• Antibiotic treatment should be tailored to Gram stain, culture, and sensitivity

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results when available
 Group A streptococcal or other beta-hemolytic streptococcal infection – Penicillin plus
clindamycin
 Clostridial infection – Penicillin plus clindamycin .
 Polymicrobial infection – Vancomycin plus a beta-lactam-beta-lactamase inhibitor.
• Antibiotics should be continued until no further debridement is needed and
the patient's hemodynamic status has normalized; this duration must be
tailored to individual patient circumstances
• Hemodynamic support — Hemodynamic instability may require aggressive 52
supportive care with fluids and vasopressors. Intravenous fluid requirements
may be high, and albumin replacement may be required in the setting of
 OUTCOME

• Necrotizing infection is associated with considerable mortality,

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even with optimal therapy.
Polymicrobial (type I) necrotizing fasciitis – 21 percent

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Monomicrobial (type II) necrotizing fasciitis – 14 to 34 percent
• Factors associated with increased mortality include
 White blood cell count >30,000/microL; band neutrophils >10
percent
 Serum creatinine >2.0 mg/dL (177 mmol/L)
 Age >60 years
 Streptococcal toxic shock syndrome
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 Clostridial infection
 Delay in surgery for more than 24 hours
Surgical Site Infections
• Superficial SSIs
Skin and subcutaneous tissue; 60% to 80% of all SSIs
• Deep Incisional SSIs
Fascia
Muscle layers
• Organ or space SSIs
Body organs
Body spaces
Eg. intra-abdominal abscesses, empyema etc...
 93% of SSI-related mortalities
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Classification of surgical
wounds
Wound class Definition Examples Wound infection
rate(%)

I. Clean Surgical incision Thyroidectomy 2

II. Clean Involves GIT, GUT or Cholecystectomy 4 - 10

contaminated respiratory tract

III. Contaminated Fresh traumatic Stab injury 20

wounds Unprepared colon
Spillage of GIT resection
contents
IV. Dirty Old traumatic Peritonitis >30
wound, perforated Resection of 55
viscus, pus necrotized tissue
Cause and risk factors
• Three major determinants of SSI
• Bacterial factors: Bacterial number, virulence, and
antimicrobial resistance ,Remote site infection, Duration of the
procedure, Wound class etc…

• Local wound factors :Surgical technique, Hematoma/seroma,

Necrosis, Sutures, Foreign bodies, Drains

• Patient factors : Age ,Steroids, Malignancy,

Immunosuppression, Obesity, Malnutrition, Diabetes

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 Abdominal trauma 04/03/2024
57
Prevention

• Three milestones in preventing SSI

I. The aseptic and antiseptic techniques

II. The proper use of prophylactic antibiotics
III. Optimize and maximize the patient's own ability to prevent
infection.

• N.B >> Microorganisms are a necessary part of the human

microenvironment, and even clean wounds have small
numbers of bacteria present at the end of the operation.
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Preventive Measures for SSI
• Preoprative:
 Shorten hospital stay
 Shower the night before
 Hair removal in the OR
 Treat remote site infection
 Prophylaxis antibiotics
 Quit smoking for >2wks
 Tight glucose control
 Optimize nutrition

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Cont…
• Intraoperative:
 Optimize OR environment
 Properly sterilized instruments and drapes
 Proper scrubbing and use of appropriate barriers
 A good surgical techniques
 Adequate warming, oxygenation, Iv fluid and glucose control

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Cont…
• Postoperative:
 Proper wound dressing
 Early drain removal ?
 Early physiotherapy
 Enteral nutrition?
 Glucose control

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 Prophylactic antibiotics
• General principles:
• Indicated when infection is either frequent or with severe outcome
• Should be effective against the most likely microbes and low toxicity
• Should be given IV route 30-60’ before incision
• Repeat the dose if procedure lasts longer than t1/2 of the drug
achieving therapeutic serum levels throughout the operative period
• No need beyond 24hrs

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Cont…
INDICATIONS:
1. Surgery that involve GIT and GUT
2. Cardiac procedures
3. Vascular surgery
4. Amputation of an extremity
5. Craniotomy
6. Implantation of prosthetic material
7. Any wound with known gross bacterial contamination
8. Accidental wounds with heavy contamination and tissue damage
9. Extensive devitalization of muscle
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 Abdominal trauma 04/03/2024
64
Cont…
• Prophylactic antibiotic is ineffective in continuing
contamination;
• 1. tracheostomies or tracheal intubation
• 2. indwelling urinary catheters
• 3. indwelling central venous lines
• 4. wound or chest drains
• 5. most open wounds, including burn wounds

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• Misuse of antimicrobial agents is associated with
• An enormous financial impact on health care costs,
• Adverse reactions due to drug toxicity and allergy,
• The occurrence of new infections such as Clostridium difficile
colitis, and
• The development of multiagent drug resistance among
nosocomial pathogens.

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Treatment
• A complete assessment of commonly recognized sites;
• wound,
• respiratory system,
• urinary tract, and
• IV access sites for evidence of infection.

• Five Ws: wind , water, wound(w abscess), walking and wonder

drug , wing/water way

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 Cont…
• Standard principles of management for all surgical infections:
Source control
 Draining an abscess, resecting or débriding dead tissue, diverting
bowel, relieving obstruction, and closing a perforation.

 The use of antibiotics is not the standard for treatment of incisional

SSI.
Reading assignment
 Intra-Abdominal Infections
Organ-Specific Infections
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